The perception of pain is a natural response to tissue injury or trauma. In a normal patient, pain is perceived at the time of injury and is resolved over time as the injury heals. In contrast, neuropathic pain, or peripheral neuropathy, is a disease of the peripheral nerves typified by a chronic or protracted state of pain that continues long after a tissue injury has healed. Like a normal state of pain, peripheral neuropathy is typically caused by acute tissue injury or trauma, however, in the case of neuropathic pain, the nerve fibers themselves are damaged in addition to the tissue, and this damage causes the nerve fibers to function incorrectly. For example, acute damage or trauma to the nerves of the peripheral or central nervous systems can cause individual nerve fibers in those systems to misfire and produce spontaneous signals they would not ordinarily produce (e.g. that are not in response to any normal stimulus) and that the brain and spinal cord do not normally receive. These spontaneous signals are abnormal and, in the case of neuropathy, are perceived by the patient as pain. Because these spontaneous signals typically continue long after the tissue injury or trauma has healed, it is the nervous system itself that is the cause of neuropathic pain, rather than any tissue injury.
Neuropathic pain can be perceived as a steady burning, as a “pins and needles” sensation, as an “electric shock,” or as other, similar sensations of pain. In some cases, peripheral neuropathy can result in numbness and abnormal sensations such as dysesthesias (impairment of sensations) and allodynias (exaggerated responses to otherwise non-noxious stimuli), that occur either spontaneously or in reaction to external stimuli. Therefore, neuropathic pain is markedly different in perception and sensation from the ordinary, acute pain that is induced by tissue trauma, such as stubbing a toe or cutting a finger. This difference arises because ordinary pain, or acute pain, which is caused by tissue injury or trauma, is nociceptive in nature (e.g. is caused by a pain stimulus), biologically self-limiting, and serves a protective biological function by acting as a warning of ongoing tissue damage. In contrast, neuropathic pain serves no biological protective function at all; rather than being a symptom of trauma or disease, the pain experienced by the patient is itself the disease. Neuropathic pain is notoriously difficult to treat and tends to respond poorly to standard pain treatments such as analgesics; in some cases even strong opioid or narcotic analgesics such as morphine, codeine and fentanyl, provide limited relief. Neuropathic pain has also been known to worsen over time, rather than improve, making treatment even more challenging for health care providers. Additionally, if chronic neuropathic pain is inadequately treated, other symptoms can develop as a result of the neuropathy apart from those associated with the perception of pain, including chronic anxiety, fear, depression, sleeplessness and impairment of social interaction. In some patients, severe neuropathic pain has even led to physical disability.
The mechanisms of action of neuropathic pain are typically complex and can involve both peripheral and central nervous system pathophysiology. The underlying dysfunction, or cause of the neuropathic state of pain, may involve deafferentation (the elimination or interruption of sensory nerve impulses) within the peripheral nervous system (e.g. neuropathy), deafferentation within the central nervous system (e.g. post-thalamic stroke) or an imbalance between the two systems. An example of neuropathic pain caused by the latter instance, an imbalance between the peripheral and central nervous systems, is the disease state commonly known as “phantom limb syndrome,” where a patient has experienced an injury or trauma that has resulted in the loss of a limb, or has had a limb surgically removed. In this case the damage caused to the nerves that originally served the missing limb causes those nerves to malfunction or misfire as described above, which in turn causes the patient's brain to perceive pain in a limb that is no longer present.
Peripheral nerve stimulation (“PNS”) was developed as a method for managing chronic or protracted pain in the extremities and has been used as a treatment for neuropathic pain since 1965. PNS uses artificial means, such as electrical impulses, to stimulate the nerves involved in the generation of neuropathic pain, which can include both the nerves involved in the nociceptive pain response and the nerves involved in non-pain, sensory responses (e.g. touch) at the location of the neuropathy, and has been found to reduce the symptoms of neuropathic pain perceived by the patient, sometimes significantly. Several theories as to how and why PNS causes relief from neuropathic pain in some individuals exist, with the generally accepted theory being that, by artificially stimulating the damaged or injured neurons or nerve fibers that cause neuropathic pain, the damaged neurons become desensitized and the pain signals that are sent by those neurons become blocked or down-regulated. The artificial stimulation employed in PNS can range greatly, from large artificial stimuli to small stimuli, but will most typically be used in a range that stimulates the neuropathic pain-causing neurons at a level that is below their minimum threshold firing value. This is done by applying an electrically stimulating signal to an individual nerve or to a bundle of nerve fibers at a level that is above their biological resting potential value, but that is not high enough to trigger depolarization and neuronal firing, in an attempt to decrease the firing sensitivity of those nerves, or to desensitize them to all stimuli so that they transmit fewer signals. For example, the use of PNS to artificially stimulate large, myelinated touch and pressure responsive nerve fibers is theorized to prevent the perception of neuropathic pain generated by those neurons by interfering with their pain signal transmissions and causing those nerve fibers to send non-painful “touch” signals to the brain in their place. While this does not remove the abnormal sensation altogether, it does serve to remove the pain.
PNS is typically performed by placing electrodes along the course of the nerves that are generating neuropathic pain and then using those electrodes to artificially stimulate the neuropathic pain-causing nerves in order to attenuate or control the transmission of pain signals generated. Several devices have been created to perform this task that employ these types of electrodes and they are an extremely safe, efficient, and effective way to ameliorate a variety of severe neuropathic pain conditions. The electrical current generated by the electrodes along the course of the neuropathic nerves effectively tricks the brain into attenuating the painful signals that are being spontaneously generated by the damaged neurons, which causes relief from the neuropathic pain. As a result, most patients are able to reduce or discontinue pain medications after having received PNS. Once the electrodes are put in place, they are used to administer a weak electrical current to the nerve or nerves of interest. In practice, this is typically performed as a two-step process. First, a temporary or trial electrode is put in place along the neuropathic pain-generating nerves and left for a brief period of time so that the patient or health care provider can perform one or more test runs to determine whether PNS will be effective for that patient. The temporary electrode is connected to a power supply outside of the patient that may be controlled by the patient or the health care provider, as appropriate, while PNS is administered to that patient on a trial basis. In the event that PNS is not helpful to the patient, the temporary electrode is removed and the treatment discontinued. If, however, it is found that PNS is providing the patient with relief from neuropathic pain, the temporary electrode is replaced with a permanent electrode that is connected to a power source that is typically surgically implanted inside of the patient, such as a battery pack similar to a pacemaker battery. Once the permanent electrode is in place, the patient may resume the activities of daily living.
Several types of electrodes have been developed for use in performing PNS. Some perform PNS by passing an electric current, and thus providing neurostimulation, through the skin. This form of PNS is called transcutaneous electronic nerve stimulation (“TENS”) and is typically accomplished by placing small electrodes topically along the path of the neuropathic pain-generating nerves, on the skin of the patient. TENS therefore has the obvious benefits of being noninvasive and readily adjustable in that the electrodes may be moved, replaced, and relocated along the skin of the patient quickly and easily. In spite of these benefits, however, many patients that have been treated with TENS experience an inadequate or minimal amount of pain relief or worse, experience no pain relief at all. Additionally, even though the electrodes themselves may be small in size and moved with relative ease, many of the accompanying devices necessary to administer TENS to patients are bulky, cumbersome, and non-portable, making TENS impractical for use in ordinary life. Further, because the electrodes are placed topically, the use of TENS precludes contact with water during treatment, thereby preventing patients from enjoying many aspects of normal, daily life without experiencing neuropathic pain.
Other treatment methods using PNS accomplish the desired neurostimulation by surgically implanting electrodes directly to and along the patient's spinal cord. This form of PNS is called spinal cord stimulation (“SCS”) and it typically uses a small lead wire as the electrode, which is connected to a power source and surgically implanted to the desired location along the spinal cord. While this procedure has been shown to be medically efficacious in some patients in the relief or reduction in the pain experienced by peripheral neuropathy, it suffers from a unique disadvantage in that several patients question the need to have a spinal procedure performed in order to control limb pain and therefore opt not to receive this form of treatment. An additional, more troubling disadvantage to SCS is that the use of electrodes along the spine and/or spinal nerves of a patient can result in broad electrical coverage regardless of the amount of electrical current delivered, which can result in several nerves being stimulated beyond those causing the neuropathic pain. As may be appreciated, this may induce abnormal sensations at bodily locations that are not damaged or that are otherwise non-painful, because other spinal nerves apart from those generating the neuropathic pain are being stimulated. Because of this, it is often necessary for the health care provider to decrease the amount of electrical current delivered to the spine during SCS in order to minimize the perception of abnormal sensations in non-affected areas. The unfortunate effect of this is that the decreased electrical current also limits the efficacy of SCS, causing the patient to experience limited pain relief. A further disadvantage to SCS is the surgical procedure that is required to accurately place the wire electrodes along the spine. When performing this procedure, it is necessary for the health care provider to accurately place the electrodes so that they stimulate the nerves generating the neuropathic pain, but they must also be properly anchored so that they remain in place after implantation. The disadvantage arises because the techniques traditionally used to anchor the wire electrodes used in SCS in place are imprecise and the electrodes have a tendency to migrate away from their point of surgical implantation in response to minimal pulling forces, such as normal bodily movement, which can lead to several problems with continued pain modulation and can cause electrical stimulation in non-desired areas and of non-desired tissues.
Nothing herein is to be construed as an admission that the present invention is not entitled to antedate a patent, publication or invention by another by virtue of prior invention.